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PubMed2006

Lung toxicity of nitrogen mustard may be mediated by nitric oxide and peroxynitrite in rats.

Nitric oxide (NO) has previously been shown to be responsible for nitrogen mustard (NM)-induced tissue toxicity. Excessive amounts of NO are known to be able to produce peroxynitrite, an important reactive nitrogen compound, by reacting with superoxide. Previous studies reported that NO synthase inhibitors are able to prevent NM toxicity. The aim of this study was to evaluate whether peroxynitrite is also responsible for NM-induced lung tissue damage in rats. Wistar rats were divided into four groups. NM was injected intratracheally and was treated with the selective inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (AG) (intraperitoneal) or the peroxynitrite scavenger ebselen (intragastric). Control animals were exposed to saline only. NM injection caused both oxidative and nitrosative stress, reflected by dramatically increased levels of the lipid peroxidation end product malondialdehyde (MDA), iNOS activation and urine nitrite-nitrate (NOx) values. Histopathological evaluation demonstrated lung damage with NM exposure. AG blocked iNOS activation and decreased urine NOx levels, and resulted in less histopathological changes in the lung. Although the histopathological outcome was found to be similar to AG, ebselen did not change urinary NOx or lung iNOS levels. Furthermore, ebselen was more able than AG to protect against MDA accumulation. In conclusion, the ability of ebselen to prevent against lung damage without blocking NO synthesis suggests that peroxynitrites may have an important role in the pathogenesis of NM toxicity in addition to NO.

Alkylating Agents↗
PubMed1986

Proton magnetic resonance (PMR) spectroscopic determination of mechlorethamine hydrochloride for injection in commercial unit doses.

A simple PMR spectroscopic method was developed for the quantitative determination of mechlorethamine hydrochloride for injection in commercial unit doses. Deuterium oxide was used as the PMR solvent and tert-butyl alcohol served as the internal standard. The mean +/- SD% recovery value of mechlorethamine hydrochloride from synthetic formulations was 99.5 +/- 0.83, with a coefficient of variation of 0.83%. The mean content of mechlorethamine hydrochloride in a group of ten commercial unit doses was 99.3% by the PMR method and 99.4% by the titrimetric method of U. S. P. XX.

Chemical Phenomena↗